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TABLE OF CONTEN TS

Introduction 1

Can We Prevent Complex Diseases Like AD? 1

AD Risk Factors We Cant Control 3

The Search for AD Prevention Strategies 5

Other Clues to AD Prevention 20

Other Areas of Research 27

So, What Can You Do? 29

For More Information 31

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Introduction

Newspapers, magazines, the Internet, and TV seem to be

full of stories about ways to stay healthy, eat right, and

keep fit. Many people are concerned about staying healthy

as they get older. Along with keeping their bodies healthy,

they want to keep their minds sharp. They also want to

avoid brain diseases, such as Alzheimers disease (AD), that

occur more often in older people than in younger people.

Currently, AD has no known cure, but the results of

recent research are raising hopes that someday it might

be possible to delay the onset of AD, slow its progress, oreven prevent it altogether. Delaying by even 5 years the

time when AD symptoms begin could greatly reduce the

number of people who have this devastating disease. The

National Institute on Aging (NIA), part of the National

Institutes of Health at the U.S. Department of Health

and Human Services; other Government agencies; and

private-sector groups support research that takes manydifferent approaches to studying how to prevent or delay

the disease.

Can We Prevent Complex DiseasesLike AD?

Many diseases, such as diabetes, heart disease, andarthritis, are complex. They develop when genetic,

environmental, and lifestyle factors interact to cause

disease and/or make it worse. The importance of these

factors may be different for different people.

AD is one of these complex diseases. It develops over many

years and appears to be affected by a number of factors that

may increase or decrease a persons chances of developing

the disease. These factors include genetic makeup, environ-

ment, life history, and current lifestyle. We cant control

some of these risk factors, but we can control others.

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AD Risk Factors We Cant Control

AgeAge is the most important known risk factor for AD. The

risk of developing the disease doubles every 5 years after

age 65. Several studies estimate that up to half of all

people older than 85 have AD. These facts are significant

because of the growing number of people 65 and older.

A 2005 Census report estimates that the number of

Americans 65 and older will more than double to about

72 million by 2030. Even more significant, the group with

the highest risk of ADthose older than 85is the fastest

growing age group in the United States.

GeneticsGenetic risk is another factor that a person cant control.

Scientists have found genetic links to the two forms of

ADearly-onset and late-onset.

Early-onset AD is a rare form of the disease, affectingonly about 5 percent of all people who have AD. It devel-

ops in people ages 30 to 60. In the 1980s and early 1990s,

researchers found that mutations (permanent abnormal

changes) in certain genes cause most cases of early-onset

AD. If a parent has any of these genetic mutations, his

or her child has a 50-50 chance of inheriting the mutated

gene and developing early-onset AD.

Late-onset AD, the much more common form of the

disease, develops after age 60. In 1992, researchers found

that three forms, or alleles (e), of a gene called apolipo-

protein E (APOE) can influence the risk of late-onset AD:

APOE e2, a rarely occurring form, may provide some

protection against AD.

APOE e3, the most common form, plays a neutral role,

neither increasing nor decreasing risk.

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APOE e4, which occurs in about 40 percent of all

people who develop late-onset AD and is present in

about 25 to 30 percent of the population, increases

risk by lowering the age of onset. Having this allele

does not mean that a person will definitely developAD; it only increases risk. Many people who develop

AD do not have an APOE e4 allele.

Researchers think that at least half a dozen other risk-

factor genes exist for late-onset AD and are intensively

searching for them. In 2007, they found another likely

risk-factor gene called SORL1. When this gene is active

at low levels or in an abnormal form, levels of harmful

beta-amyloid increase in the brain. Beta-amyloid is a

component of amyloid plaques, one of the hallmarks of

AD. Interestingly, the SORL1 gene also was identified as

a risk-factor gene for certain aspects of cognitive decline,

suggesting that cognitive decline and AD may share at

least one predisposing genetic factor.

To Learn More

For more information about AD and AD genetics, visit the

Alzheimers Disease Education and Referral (ADEAR) Center

website at www.nia.nih.gov/Alzheimers. The ADEAR Center

offers free publications, such as theAlzheimers Disease Fact

Sheet, theAlzheimers Disease Genetics Fact Sheet, and

Alzheimers Disease: Unraveling the Mystery.

Finding AD risk-factor genes is essential for understand-

ing the very early biological steps that lead to the vast

majority of AD cases and for developing drugs and other

prevention and treatment strategies. Finding these genes

also will help scientists develop better ways to identifypeople at risk of AD and determine how the genes may

interact with other genes or with lifestyle or environmen-

tal factors to affect an individuals AD risk.

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The Search for AD PreventionStrategies

We cant do much about our age or genetic profile, but

scientists are working hard to understand a variety ofother factors that may be involved in the disease. Some

scientists are examining the biological bases for AD. This

research might lead to the development of drugs that

could protect against or block biological processes leading

to cognitive decline and AD.

Other scientists are studying health, lifestyle, and en-

vironmental factorssuch as exercise and diet or thecontrol of chronic diseases like diabetesthat may play

a role in preventing or slowing AD or cognitive decline.

Recent research suggests that maintaining good overall

health habits may help lower our chances of developing

several serious diseases, including brain diseases such as

AD. This area is of particular interest because it appears

that there may be things that individuals can do them-selves to hold off AD.

Several of these potential factors have been identified

in animal studies and in epidemiologic studies (studies

that compare the lifestyles, behaviors, and characteristics

of groups of people). At present, these factors are only

associated with changes in AD risk. Further research,especially clinical trials, will be needed to determine

cause-and-effectwhether these factors really do help

prevent cognitive decline or AD directly.

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Understanding Scientific Findings in the News

It can be hard to know what to conclude about scientific

study findings. Knowing how the study was conducted

can help put the results into the right perspective.

One main type of research is the epidemiologic study.

These studies are observationalthey gather information

about people who are going about their daily lives. Study

participants follow many behaviors and practices. It is

difficult, therefore, to determine the exact benefits or risks

of one particular behavior from among all the healthy or

harmful things that may happen to participants or that theydo. That is why, in epidemiologic studies of AD, scientists

will say that a finding is associated with AD, or not. The

epidemiologic evidence linking a behavior and AD is, at

best, suggestive, but we do not know that the behavior by

itself actually helps to cause or prevent AD.

Other types of researchtest-tube studies and studies in

animalsadd to the findings from epidemiologic studies.Scientists sometimes use these studies to control factors

that might otherwise influence a research result. Control-

ling specific factors allows scientists to be more certain

about why they get the results they do. It also allows

them to describe their results more precisely. Of course,

showing a cause-and-effect relationship in tissue samples

or even in animal studies does not mean that the relation-ship will be the same in humans.

Clinical trialsresearch studies in humans that rigorously

test safety, side effects, and how well a medication or

behavioral treatment worksare the gold standard for

research. Clinical trials are used to determine whether a

specific medication, device, or treatment actually prevents

or delays AD.

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Assessing Physical ActivityAccumulating evidence suggests that physical activity may

be good for our brains as well as our hearts, waistlines,

and ability to carry out activities of daily living. Epide-

miologic studies have found associations between physicalactivity and improved cognitive skills or reduced AD risk.

For example, investigators looked at the relationship of

physical activity and AD risk in about 1,700 adults aged

65 years and older over a 6-year period. They found that

the risk of AD was 35 to 40 percent lower in those who

exercised for at least 15 minutes 3 or more times a week

than in those who exercised fewer than 3 times a week.

Scientists have sought to confirm these associations in

animal studies, hoping to clarify why physical activity

might be related to reduced risk of cognitive decline and

AD. For example, studies in older rats and mice have

found that exercise increases the number of small blood

vessels that supply blood to the brain and increases

the number of connections between nerve cells. Other

research has shown exercise to raise the level of specific

brain-growth factors in an area of the brain that is

particularly important to memory and learning.

Both epidemiologic and animal studies point to associa-

tions and help to explain them. However, epidemiologic

studies cant tell us whether a true cause-and-effectrelationship exists between a particular factor and

AD risk. For example, people who exercise tend to be

healthier in other ways, such as having decreased rates of

heart disease or diabetes. They may also have healthier

lifestyles, such as eating a nutritious diet. This means that

even if people who exercise are less likely to develop AD,

we dont know whether this is due to the exercise or themore healthful eating or other lifestyle differences that

distinguish them from inactive people.

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Likewise, animal studies cant tell us whether an in-

tervention will definitely work in humans. Thats why

investigators conduct clinical trialscontrolled studies

involving humans. Clinical trials are the most reliable

method for showing whether intervention strategiesreally can work to prevent or treat AD in people. This

is because clinical trial participants are randomly

assigned to receive or not receive a treatment (for

example, exercise). Therefore, any differences between

the groups should be due to the exercise program rather

than other differences between the groups.

NIA supports clinical trials related to exercise and

cognitive function. One completed trial used functional

magnetic resonance imaging (MRI) tests to measure

changes in brain activity in older adults before and after

a 6-month program of brisk walking. Results showed that

brain activity increased in specific brain regions as the

participants cardiovascular fitness increased. A similar

study showed that brain volume increased as a result of

a walking program.

These findings strongly suggest a biological basis for the

role of aerobic fitness in helping to maintain the health

and cognitive functioning of adults as they age, at least in

the short term. Currently, a trial is underway to look at

the effects of a 1-year aerobic fitness training program oncognition and brain activity and structure in older adults.

Other NIA-supported research is examining whether

exercise can delay the development of AD in people with

mild cognitive impairment (MCI).

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Exploring Dietary FactorsA number of studies suggest that how we eat may be

linked to our risk of developingor not developingAD.

This is another important area of current AD research.

A nutritious dieta diet that includes lots of fruits,vegetables, and whole grains and is low in fat and added

sugarcan reduce the risk of many chronic diseases,

including heart disease, type 2 diabetes, and obesity. Ani-

mal studies, epidemiologic studies, and clinical trials are

looking at whether a healthy diet also can help preserve

cognitive function or even reduce AD risk.

Studies have examined foods that are rich in antioxidants

and anti-inflammatory components to find out whether

those foods affect age-related changes in the brain. One

study found that curcumin, the main ingredient of tur-

meric (a spice used in curry), can suppress the build-up of

harmful beta-amyloid in the brains of rodents. Another

study, in AD transgenic mice (those that are specially

bred to have features of AD), found that DHA (docosa-

hexaenoic acid, a type of omega-3 fatty acid found in some

fish) reduced the presence of beta-amyloid and plaques.

Other research has shown that older dogs perform better

on learning tasks when they eat a diet rich in antioxidants

and live in an enriched environment with many oppor-

tunities to play and interact with others.

In addition, studies in rats and mice have shown that

dietary supplementation with blueberries, strawberries,

and cranberries can improve cognitive function, both

during normal aging and in animals that have been bred

to develop AD. Scientists are beginning to identify some

of the chemicals responsible for these berries beneficial

effects and think that the chemicals may act by neutral-izing free radicals. This may reduce inflammation or

stimulate neurons to protect themselves better against

some of the adversities of aging and AD.

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Several epidemiologic studies have shown an association

between eating a diet rich in vegetables (especially green

leafy vegetables and cruciferous vegetables like broccoli)

and a reduced rate of cognitive decline. Researchers

speculate that the beneficial effect may come from theantioxidant and folate content of the vegetables.

These results are interesting, but in their normal daily

lives, people typically consume many different foods and

nutrients. With this in mind, some investigators have con-

ducted epidemiologic studies to examine a groups entire

dietary pattern. One of these studies showed a reduced

risk of AD in those who ate the Mediterranean diet

a diet that includes many fruits, vegetables, and beans;

moderate amounts of fish; low-to-moderate amounts of

dairy foods; small amounts of meat and poultry; regular

but moderate amounts of wine; and olive oil.

These kinds of findings are exciting and suggestive, but

they are not definitive. To confirm them, NIA is supportingseveral clinical trials to examine the relationship between

specific dietary components and cognitive decline and AD.

Investigating Chronic DiseasesFor some years now, scientists have been finding clues

that damage to the vascular system (the bodys vast

system of large and small blood vessels) may contributeto the development of AD or affect its severity. Several

common chronic diseases that affect older people, in-

cluding heart disease, stroke, and type 2 diabetes, also

affect the bodys vascular system and have been tied to

declines in cognitive function or increased AD risk. In

addition, heart disease, high blood pressure, and diabetes

to a large extent can be modified by diet, exercise, andother lifestyle changes. Therefore, scientists are keenly

interested in learning whether reducing the risks of or

controlling these conditions through lifestyle changes

also may reduce the risks of cognitive decline or AD.

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Much of the evidence so far about possible relationships

between vascular diseases and cognitive decline or

AD risk comes from epidemiologic studies. To clarify

and build on these findings, scientists have conducted

a variety of studies, including test tube, animal, andadditional epidemiologic studies. NIA is supporting

several clinical trials, including a trial to test the effect

of lowering blood pressure and blood cholesterol levels

on cognition in people with diabetes. Several other trials

are examining whether intensive diabetes treatment can

reduce cognitive decline. Researchers are also looking at

increased stiffness of blood vessels with age as anotherpotential treatment target.

Examining Social Engagement and IntellectuallyStimulating ActivitiesObservations of nursing home residents and older people

living in the community have suggested a link between

social engagement and cognitive abilities. Having manyfriends and acquaintances and participating in many

social activities also is associated with reduced cognitive

decline and decreased risk of dementia in older adults.

For example, the NIA-funded Chicago Health and Aging

Project showed that more social networks and a higher

level of social engagement were associated with a higher

level of cognitive function at the beginning of the study.These factors also were related to a reduced rate of

cognitive decline over time.

Studies have also shown that keeping the brain active is

associated with reduced AD risk. In the Religious Orders

Study, for example, investigators periodically asked more

than 700 participantsolder nuns, priests, and religious

brothersto describe the amount of time they spent in

seven information-processing activities. These activities

included listening to the radio, reading newspapers,

playing puzzle games, and going to museums. After

following the participants for 4 years, the investigators

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found that the risk of developing AD was 47 percent

lower, on average, for those who did the activities most

often than for those who did them least frequently.

Other studies have shown similar results. In addition, a

growing body of research suggests that, even in the pres-

ence of AD plaques, the more formal education a person

has, the better his or her memory and learning abilities.

Another NIA-funded study supports the value of lifelong

learning and mentally stimulating activity. It showed that

during early and middle adulthood, cognitively healthy

older people had engaged in more mentally stimulatingactivities and spent more hours doing them than did those

who ultimately developed AD. Other studies have shown

that people who are bilingual or multilingual seem to

develop AD at a later age than do people who only speak

one language.

The reasons for this apparent link between social engage-

ment or intellectual stimulation and AD risk arent entirely

clear, but scientists suggest four possibilities:

Such activities may protect the brain in some way,

perhaps by establishing cognitive reserve. (Cogni-

tive reserve is the brains ability to operate effectively

even when some function is disrupted or the amount

of damage that the brain can sustain before changesin cognition are evident.)

These activities may help the brain become more

adaptable and flexible in some areas of mental function

so that it can compensate for declines in other areas.

People who engage in these activities may have other

lifestyle factors that protect them against developingAD.

Less engagement with other people or in intellectu-

ally stimulating activities could be the result of very

early effects of the disease rather than its cause.

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The only way to really evaluate some of these possibili-

ties is to test them in a controlled way in clinical trials.

Several clinical trials have examined whether memory

training and similar types of mental skills training

can actually improve the cognitive abilities of healthyolder adults and people with mild AD. In the Advanced

Cognitive Training for Independent and Vital Elderly

(ACTIVE) trial, for example, certified trainers provided

10 sessions of memory training, reasoning training, or

processing-speed training to healthy adults 65 years old

and older. The sessions improved participants mental

skills in the area in which they were trained. Even better,these improvements persisted for up to 5 years after the

training was completed.

The Cognitive and Emotional Health Project

The National Institute on Aging (NIA) has primary

responsibility for research on AD and age-related

declines in mental skills (also called cognitive skills),such as remembering, learning, thinking, decision

making, and language. This responsibility is part of a

larger mission to understand the nature of aging and

find ways to help people stay physically, emotionally,

and cognitively healthy for as long as possible.

Several years ago, NIA, the National Institute of Mental

Health, and the National Institute of NeurologicalDisorders and Stroke launched the Cognitive and

Emotional Health Project (http://trans.nih.gov/CEHP).

This project has begun to identify and describe what

we know about the diverse factors that may affect

the emotional health and cognitive abilities of adults.

Research on the most promising factors is being carried

out to determine whether any of them will result instrategies that can help people remain mentally and

emotionally vibrant as they age. The hope is that

successful strategies will also add to our knowledge

about what can be done to reduce the likelihood of

developing neurodegenerative diseases such as AD.

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Other Clues to AD Prevention

NIAs program of AD research continues to add to what

we know about AD and yield clues about possible ways

to prevent the disease. The following sections brieflydescribe a few other areas that scientists are exploring.

Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)Inflammation in the brain is a common feature of AD,

but it is unclear whether this is a cause or an effect of

the disease. Some epidemiologic studies suggest an

association between a reduced risk of AD and commonlyused nonsteroidal anti-inflammatory drugs (NSAIDs),

such as ibuprofen, naproxen, and indomethacin. So far,

clinical trials have not demonstrated a benefit for AD

from these drugs or from the newer cyclooxygenase-2

(COX-2) inhibitors, such as rofecoxib and celecoxib.

However, scientists continue to look for ways to test how

other anti-inflammatory drugs might affect the develop-ment or progression of AD.

AntioxidantsDamage during aging from highly active molecules called

free radicals can build up in nerve cells and result in a

loss of cell function, which could contribute to AD. Some

population and laboratory studies suggest that antioxi-dants from dietary supplements or food may provide

some protection against this damage (called oxidative

damage), but other studies show no effect.

Clinical trials may provide some answers. Several cur-

rent trials are investigating whether antioxidants, such

as vitamins E and C, alpha-lipoic acid, and coenzyme Q,

can slow cognitive decline and development of AD.

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NIA-sponsored sub-studies to ongoing trials have looked

at whether two treatments provide any protection against

cognitive decline in women. One sub-study tested low-

dose aspirin and antioxidant supplementation in healthy

women, and the other tested antioxidant and folate sup-plements in women who already had heart disease. Initial

results indicate that aspirin may provide some benefits for

maintaining executive function but has no impact on other

cognitive domains. For vitamin E, there was no overall

benefit. Analysis of these studies is ongoing.

Another study added to a prostate cancer prevention trial

is examining whether taking vitamin E and/or selenium

supplements over a period of 7 to 12 years can help pre-

vent memory loss and dementia. Although the primary

trial was stopped because the supplements were shown

not to prevent prostate cancer, researchers are continu-

ing to follow participants to analyze longer term effects

of the supplements.

The Memory Impairment Study compared the use of

donepezil (Aricept), vitamin E supplements, or placebo

(an inactive substance) in participants with mild cogni-

tive impairment (MCI) to see whether the drugs might

delay or prevent progression to AD. People with MCI

have more memory problems than normal for people

their age, but their symptoms are not as severe as thosewith AD. More people with MCI, compared with those

without MCI, go on to develop AD. The study found that

taking vitamin E had no effect on progression to AD. It

may be that this antioxidant did not help after memory

declines had already started. Donepezil seemed to delay

progression to AD during the first year of treatment;

however, by the end of the 3-year study there was nobenefit from the drug. The U.S. Food and Drug Adminis-

tration (FDA) has not approved donepezil for treatment

of MCI.

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EstrogenThe hormone estrogen is produced by a womans ovaries

during her childbearing years, and its production

declines dramatically after menopause. Over the past

25 years, some laboratory and animal research, as wellas observational studies in women, have suggested that

estrogen may protect the brain. Experts have wondered

whether taking estrogen supplements could reduce the

risk of AD or slow disease progression.

A number of clinical trials have shown that estrogen does

not slow the progression of already-diagnosed AD and is

not effective in treating or preventing AD if treatment is

begun in later life. For example, a large trial found that

women older than 65 who took estrogen (Premarin) alone

or estrogen with a synthetic progestin (PremPro) were

actually at increased risk of developing dementia, including

AD. However, some questions, such as whether other forms

of estrogen or starting treatment nearer menopause might

be more effective, remain unanswered. These questions are

now being investigated in clinical trials.

Researchers also are probing estrogens possible beneficial

effects on the brain. For example, scientists have developed

estrogen-like molecules called SERMs (selective estrogen-

receptor modulators) that protect against bone loss and

other consequences of estrogen loss after menopause. Thesemolecules may retain estrogens neuron-protecting ability

but may not have some of its other harmful effects on the

body, such as increasing the risk of uterine cancer. One

large clinical trial showed that raloxifene, a SERM used to

prevent and treat osteoporosis and to reduce the incidence

of breast cancer in women at high risk for the disease,

lowered the risk of MCI in a group of postmenopausalwomen with osteoporosis. Another clinical trial is testing

whether raloxifene can slow the rate of AD progression.

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ImmunizationCould a vaccine someday prevent AD? Early vaccine

studies in mice were so successful in reducing deposits

of beta-amyloid and improving brain performance on

memory tests that investigators conducted preliminaryclinical trials in humans with AD. These studies had to

be stopped because life-threatening brain inflammation

occurred in some participants. However, scientists are

continuing to refine this strategy in animal models of AD,

hoping to find ways of maintaining the vaccines beneficial

effects while reducing the unwanted side effects. Several

pharmaceutical companies have obtained permission fromthe FDA to test several of these new vaccine strategies for

safety in early-stage clinical trials.

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Technologies Help Scientists Develop DiagnosticProcedures

One important goal of AD research is to develop better

diagnostic strategies for identifying individuals who are at

high risk of developing the disease or who are at very earlystages of the disease. For example, scientists are trying to

discover whether changes in certain biological compounds

present in blood, urine, or cerebrospinal fluid could indi-

cate early AD changes in the brain. Understanding more

about these biological markers, how they work, and what

causes their levels to change is important in helping scien-

tists answer questions about what initiates AD and howit develops. Learning more about these markers also may

help scientists track whether certain medications are hav-

ing their intended effects early in the course of the disease

and may some day lead to new prevention strategies.

The use of imaging techniques, such as magnetic reso-

nance imaging (MRI) and positron emission tomography

(PET), to measure brain structure and function, is also

showing promise in AD research. An NIA public-private

partnershipthe AD Neuroimaging Initiativeis a large

nationwide study to determine whether MRI and PET

scans or other imaging or biological markers can be used

to measure changes in older participants who have MCI

or AD or who are cognitively normal. The measurements

may one day identify people early in the disease process

and also help physicians assess the response to treatment

much more rapidly and less expensively than is possible

today.

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So, What Can You Do?

Our knowledge about AD is growing rapidly as scientists

expand their understanding of the many factors involved

in this devastating disease. Although no treatments ordrugs have yet been proven to prevent or delay AD, peo-

ple can take some actions that are beneficial for healthy

aging and that also might reduce the effect of possible

risk factors for AD. For example, you can:

exercise regularly

eat a healthy diet that is rich in fruits and vegetables

engage in social and intellectually stimulating

activities

control type 2 diabetes

lower high blood pressure levels

lower high blood cholesterol levels

maintain a healthy weight

These actions lower the risk of other diseases and help

maintain and improve overall health and well-being.

However, it is important to remember that they will not

necessarily prevent or delay AD in any one person. Even

if these actions were eventually proven effective, theymight not offset a persons individual genetic and other

risk factors enough to prevent the development of AD.

Whether you have memory problems or not, you can take

one more important actionvolunteer to participate in

research. Participating in clinical trials is an effective

way to help in the fight against AD. People who par-

ticipate in these studies say that the biggest benefit is

having regular contact with experts on AD who have lots

of practical experience and a broad perspective on the

disease. They also feel they are making a valuable con-

tribution to future knowledge that will help scientists,

people with AD, and their families.

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People who are interested in joining an AD clinical trial

can visit the website of the Alzheimers Disease Educa-

tion and Referral (ADEAR) Center, a service of the NIA,

at www.nia.nih.gov/Alzheimers or call the ADEAR Center

toll-free at 800-438-4380 for a referral to the nearestparticipating study site. Visit www.nia.nih.gov/Alzheimers/

ResearchInformation/ClinicalTrials for more about AD

clinical trials.

Families interested in participating in the AD Genetics

Study can call the National Cell Repository for Alzheimers

Disease (NCRAD) toll-free at 800-526-2839. Information is

also available on the NCRAD website at www.ncrad.org.

A Final Word of Caution

Because AD is such a devastating disease, caregivers

and patients may be tempted by untried, unproven, and

unscientific cures, supplements, or prevention strategies.

Check with your doctor before trying pills or any otherprescription or non-prescription treatment that prom-

ises to prevent AD. These purchases might be unsafe or

a waste of money. They might even interfere with other

medical treatments that have been prescribed.

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For More Information

Becoming well informed is another important step you

can take to protect your health. Thousands of websites

provide health-related information, including informa-

tion on AD. Some of the information on these websites

is reliable, but some is not. Health websites sponsored

by the Federal Government are good sources of informa-

tion, as are websites of large professional organizations

and well-known medical schools. Some excellent Internet

sources of AD and other health-related information for

consumers are:

Alzheimers Disease Education and Referral

(ADEAR) Center

P.O. Box 8250

Silver Spring, MD 20907-8250

800-438-4380 (toll-free)

www.nia.nih.gov/Alzheimers

A service of the National Institute on Aging (NIA), the

ADEAR Center offers information and publications

for families, caregivers, and professionals on diagnosis,

treatment, patient care, caregiver needs, long-term care,

education and training, and research related to AD. Staff

members answer telephone, email, and written requests

and make referrals to local and national resources.

The ADEAR website offers free, online publications in

English and Spanish; email alert and online Connections

newsletter subscriptions; an AD clinical trials database;

the AD Library database; and more.

Alzheimer Research Forum

www.alzforum.org

The Alzheimer Research Forum, an online community and

resource center, offers professionals and the general public

access to an annotated index of scientific papers, research

news, moderated discussions on scientific topics, libraries

of animal models and antibodies, and directories of clinical

trials, conferences, jobs, and research-funding sources.

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Alzheimers Association

225 North Michigan Avenue, Floor 17

Chicago, IL 60601-7633

800-272-3900 (toll-free)

866-403-3073 (TDD/toll-free)www.alz.org

The Alzheimers Association is a national, nonprofit

organization with a network of local chapters that

provide education and support for people diagnosed with

AD, their families, and caregivers. The Association also

funds research on AD.

Alzheimers Disease Cooperative Study

University of California, San Diego

9500 Gilman Drive

La Jolla, CA 92093-0949

858-622-5880

www.adcs.org

The Alzheimers Disease Cooperative Study (ADCS)

is a cooperative agreement between NIA and the

University of California, San Diego, to advance research

in the development of drugs to treat AD. The ADCS is a

consortium of medical research centers and clinics working

to develop clinical trials of medicines to treat behavioral

symptoms of AD, improve cognition, slow the rate of decline

caused by AD, delay the onset of AD, or prevent the diseasealtogether. The ADCS also develops new and more reliable

ways to evaluate patients enrolled in clinical trials.

ClinicalTrials.gov

www.ClinicalTrials.gov

ClinicalTrials.gov is a registry of federally and privately

supported clinical trials conducted in the United Statesand around the world. Users can search for clinical trials

and find information about each trials purpose, who may

participate, locations, and phone numbers for more details.

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For additional copies of this publication or further

information on Alzheimers disease, please contact:

Alzheimers Disease Education and Referral

(ADEAR) Center

www.nia.nih.gov/Alzheimers

800-438-4380P.O. Box 8250

Silver Spring, MD 20907-8250

National Institutes of Health

National Institute on Aging

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U.S. DEPARTMENT OF HEALTH

AND HUMAN SERVICES

National Institutes of Health

National Institute on Aging

NIH Publication No. 09-5503

April 2009